Commercial dimeticone-containing products such as for instance sab simpler.RTM. and Lefax.RTM. (see the Rote Liste 1993) are used to treat flatulence and to prepare patients for sonography.
WO 90/07930 discloses the use of dimethylpolysiloxane, in particular in conjunction with silica gel in the treatment of diseases of the esophagus, the stomach and the duodenum, such as esophagitis, ulcera (ventriculi and duodeni) and gastrites. Said document describes the capability of dimeticone to form and maintain a protective film in the esophagus, the stomach and the duodenum after oral administration.
In recent years, it has become known that in some forms of chronic gastritis and in the development of ulcera (ulcus ventriculi and duodeni), the infection of the gastro-intestinal (GI) tract with the gram negative pathogen Hp is a pathogenetic factor, and its relationship to the genesis of gastric carcinoma is being increasingly discussed.
Although it has been known among pathologists since the close of the 19th century that spiral bacteria are present in the stomach mucosa, it was not until 1983 that Hp was cultured from bioptic material of the antrum mucosa of patients afflicted with peptic ulcera and gastritis. (Marshall, B. J.: Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet I (1983), 1273-1275).
Hp is acid-instable and sensitive to competition from other bacteria. Hence, the pathogen can only grow in a particular ecological niche. It finds this niche directly underneath the protective mucosa layer on the epithelium of the antrum and the body mucosa, but also on gastric metaplasies of the duodenal mucosa.
The route of Hp infection has not, so far, been elucidated. The infection was thought likely to be passed on orally from man to man, especially since it has not yet been possible to establish a pathogen reservoir of animal origin. The rate of infection depends on sanitation standards. In Western industrialized countries, the infection rate is about 1% per year. Hence, Hp infections are found in 60% of the persons aged 60.
The association of the Hp pathogen with different symptoms of the upper GI tract was systematically investigated in the past few years. The high prevalence of Hp infection in a population not afflicted with ulcus initially led to the assumption that Hp is a harmless saprophyte. Nowadays it is considered an established fact that the pathogen causes the B-type gastritis in the mucosa of the stomach. (Dixon, M. F.: Helicobacter pylori and peptic ulceration: Histopathological aspects. J. Gastroenterol. Hepatol. 6 (1991), 125-130).
The B-type gastritis is closely related to Hp infection which is detected in almost 100% of these patients.
The B-type gastritis is almost always present in patients suffering from ulcus duodeni, although the pathogenetic relationship is still unclear.
Experiences made in many years with acid blockers not possessing an antibacterial effect against Hp, have shown that ulcera can be cured even in cases of persistent Hp growth. About 10% of the patients cured from Hp by an antibacterial therapy, show an ulcus relapse within a year. Admittedly, these patients, as a rule, also suffer from an Hp re-infection. It must remain an open question why the relapse of the Hp infection in these patients is sufficient to cause an ulcus relapse within a year, when 40% of the population not afflicted with ulcera are Hp positive.
Ulcus ventriculi is also considered to be associated with Hp. In this case, the correlation with the Hp infection is not as close, as only 70-80% of the patients with gastric ulcera are Hp positive (Marshall, B. J., loc. cit.).